快速眼动睡眠的发育减少:向盐酸盐受体调节的转变

T. Kobayashi, R.D. Skinner, E. Garcia-Rill
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引用次数: 9

摘要

我们发现,在15日龄左右,足桥脑神经元的反应性从n -甲基-d-天冬氨酸(NMDA)调节转变为kainic酸(KA)调节。从出生到青春期结束,人类的快速眼动睡眠(REM)会减少50%到15%的睡眠时间,而老鼠在出生后10到30天也会出现类似的减少。细胞内记录的II型胆碱能PPN神经元,已知可调节清醒和快速眼动睡眠,在此期间对NMDA的反应性逐渐降低,对KA的反应性增加。非胆碱能PPN神经元在反应性方面没有表现出发育依赖性的变化。这些结果并不有助于解释KA和NMDA是否控制了快速眼动睡眠的发育减少,然而,数据表明,在15天的转变表明,快速眼动睡眠在成人中被KA受体选择性地调节。因此,如果开发出合适的化合物,KA受体拮抗剂可能成为快速眼动睡眠驱动增强和频繁夜间觉醒的疾病的有效治疗方法,如精神分裂症、焦虑、失眠等。
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Developmental decrease in REM sleep: the shift to kainate receptor regulation

We found a shift in the responsiveness of pedunculopontine neurons from N-methyl-d-aspartic acid (NMDA) to kainic acid (KA) regulation around 15 days of age. While rapid eye movement (REM) sleep in humans decreases from 50 to 15% of sleep time between birth and the end of puberty, a similar decrease in the rat occurs from 10 to 30 days postnatally. Intracellularly recorded type II cholinergic PPN neurons, known to modulate waking and REM sleep, showed a gradual decrease in responsiveness to NMDA, and an increase in responsiveness to KA, during this period. Non-cholinergic PPN neurons did not show a developmental-dependent change in responsiveness. These results do not help explain if KA and NMDA control the developmental decrease in REM sleep, however, the data indicate that the shift at ∼15 days suggests that REM sleep becomes selectively modulated by KA receptors in the adult. Therefore, given development of appropriate compounds, KA receptor antagonism may become an effective treatment for disorders that manifest increased REM sleep drive and produce frequent nocturnal arousals and awakenings, e.g. schizophrenia, anxiety, insomnia, etc.

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